A. Cell mediated immunity in psoriasis. We have shown that psoriatic subjects have abnormal cell-mediated immune (CMI) responses. The role these responses play in the cause/effect of psoriasis is as yet undefined. In partial definition of this we have demonstrated that mediator production by monocytes (monokines) and lymphocytes (lymphokines) as well as plasma factors are abnormal. These factors will be isolated and characterized by standard biochemical methods. Following isolation, they will be assayed for qualitative and quantitative differences by monitoring their activity in cell proliferation systems (HeLa and epidermal cell cultures), the animal model and in situ lesions, and in CMI systems (one way mixed leukocyte responses, lympyocyte blastogenesis and monocyte functions). We have also shown that monocytes from psoriatic subjects (with and without disease) are activated. Further definition of this activation will be determined by longitudinal and non-longitudinal studies of monocyte function (motility, intracellular biochemical status, and mediator release. To establish whether the monocyte can be used as an index tissue for psoriasis, determination of function relative to cyclic nucleotide levels and alterations thereof using pharmacologic probes, will be carried out. Clinical correlation will be made by isolation of factors from involved skin and noting the effects caused by the intradermal injection of isolated mediators. B. Artificial animal model for psoriasis. We have shown xenogeneically grafted skin is a useful model to study epidermal homeostasis and perturbations thereof. Studies will continue to define: a possible host vs. graft reaction; the kinetics of normal skin, involved and uninvolved psoriatic skin relative to longitudinal studies and to agents which alter homeostasis. The system will also be used as a model to study humoral factors (serum, lymphokines, monokines, etc.) as a cause/effect of psoriasis.